The energy factor is secondary

Contrary to widespread belief, the energy factor is secondary (which does not mean that it is to be disregarded) to weight gain. Epidemiological studies show that there is no correlation between calorie intake and obesity. There is even proof to the fact that the contrary is true in many cases. Since 1960, the daily average caloric intake in Western countries has decreased by approximately 35%.Notwithstanding, during the same period obesity has jumped by 400%.

Hyperinsulinism is the result of an excessive pancreatic secretion of the insulin hormone. Insulin is what lowers blood sugar levels during the course of the metabolic processes following digestion.

When we eat carbohydrates / glucidic foods (bread, pâte, potatoes, fruit, sugar…) they are transformed into glucose. Glucose passes our intestinal wall and goes into our bloodstream. This provokes glycemia peaks; increases in blood sugar levels which on an empty stomach are approximately 1g par liter of blood. Glycemia triggers insulin secretion which is what sends excess glucose into our bloodstream so that it may be stored in our liver and muscular tissue. This reverses glycemia to its original levels.

In an individual whose mechanism works in a normal fashion, insulin secretion is proportional to blood sugar levels. The insulin secreted by his body is thus that required to lower glycemia.

In some people, however, insulin response is out of proportion with regards to glycemia. This excessive insulin secretion is what is known as hyperinsulinism.

For the past 25 years, numerous scientific studies have shown that hyperinsulinismis always tied to excess weight and à fortiori to obesity. Medical researcher B. Jeanrenaud has described this process quite well: "In all cases of obseity, regardless of species and mechanism, hyperinsulinism is always present, and this hyperinsulinism is directly proportional to Body Mass Index (BMI) which measures the degree of excess weight." He adds that, "In animals, excess weight can be provoked by injecting insulin. Excess weight is reversed when the treatment is stopped."

High-GI carbohydrates are at the root of hyperinsulinism

Contrary to long-standing beliefs, one carb is not the same as another; they are not not transposable since they a do not all provoke the same metabolic response. What is more, it has been shown that they are all absorbed within the same lapse of time by our intestines and that, as a result, classifying them as fast and slow sugars is absolutely absurd and misleading.

Since the beginning of the 1980s, proof has been given to the fact that the 980 carbohydrates which fall into the same category (two complex starches like for example lentil and potatoes) can contain the same amount of calories and yet provoke totally different blood sugar levels, possibly twice to three times as high from one to the other.

In order to reflect how our bodies really respond to carbohydrates, carbs have been ranked on a scale according to their potential to raise blood sugar levels. Carbs with low GIs are those that provoke low blood sugar levels whereas carbs that provoke high sugar levels are ranked in the high GI category.

Insulin resistance

A person who occasionally consumes one or more high-GI carbs will secrete the insulin required to lower blood sugar levels. However, when a person has the habit of consuming high-GI carbs, his body generates insulin resistance (also known as low insulin sensibility). Glucose, in effect, despite inusulin secretion, will tend to stay in this person's bloodstream. This condition is known as the insulin resistance syndrome and it is particularly marked in cases of Type II diabetes.

What happens is that insulin receptors cease to function adequately and gluco--dependent cell tissues fail to recognize the presence of insulin. High sugar levels settle in as glucose builds up in our bloodstream instead of going into the cells. As a result of this inertia, our organism becomes « impatient » and orders our pancreas to secrete more insulin, that which only contributes to aggravating hyperinsulinism. This then becomes a vicious circle where hyperinsulinism ensues in insulinoresistance.

Hyperinsulinism is what makes us gain weight

As remarked by numerous authors, one of the essential properties of insulin is that it acts on fatty metabolism. This is known as lipogenesis.

Storage of fatty acids in fat reserve
Insuline, and a fortiori hyperinsulinism, stimulates enzyme activity, namely that of lipoprotein lipase. This enzyme’s function is to movilize circulating fatty acids (which correspond to fats eaten in the most recent meal) in order to stock them as triglycerides, thus increasing the volume of fat cells (adipocytes).

If the glycemia peak following a meal is way too high, the corresponding glucose will most probably exceed our body’s needs. The hyperinsulinism provoked by said hyperglycemia will, under the impulse of lipoprotein lipase, convert this residual glucose into fat which will be stored in fat cells.

Hyperinsulinism is definitely the functional cause of weight gain!

The right question to ask would be what would have become these fatty acids if they had not been stored through lipogenesis. The answer is simple, although surprising: if they had not been activated by lipoproteine lipase (because of insulin), these fatty acids wouls simply have been burned by our organism which, under these circumstances, tends to adjust metabolic performances in an adequate manner.

Weight-losing process (LIPOLYSIS)

As we can see, lipogenesis is the metabolic process which results in fat reserves, and so, in gaining weight. Lipolysis, is exactly the opposite: it is the metabolic process which results in freeing fats, and so, in losing weight.

Our organism finds itself in a situation that forces it to seek fat in fat cells les cellules graisseuses (adypocites) to use as carburant, thus reducing their volume. In order for this to work, insulin has to be low. The mechanism is as follows: low levels of insulin activate the triglyceride-lipase enzyme, which is responsible for evicting fatty acids from adipose tissues (adypocites) by bringing them into our bloodstream so that they can be used as carburant. Our organism will then try to use them (burn them) by modifying its energetic performance, according to its needs.

As a conclusion, we can say that insulin is what catalyzes weight gaining. Thus, in order to lose weight, we have to control insulin levels by trying to keep them as low as possible. To achieve this, we should try to keep after-meal (post-prandial) glycemia peaks at their lowest.

The only solution will naturally be to eat only low, and preferably very low, GI carbs. Experience indicates that, by eating solely low (35 or lower) GI carbs, insulinic response stays low enough to allow our weight-losing enzyme —triglyceride-lipase— to work and to thus provoke a weight-losing process.

The key factor to gaining weight is, as we have just seen, consuming high GI carbohydrates

The lipogenesis phenomenon, described above, explains why and how. Likewise, understanding the lipolysis phenomenon makes us aware of the fact that if we want to lose weight, we have to eat low GI carbohydrates.

We realize, however, that weight gain is not solely the result of storing the fats eaten in our meals. Insulin also affects surplus glucose resulting from excessive consumption of high GI carbohydrates.

For many years, nutritionists believed that glucose could not be converted into fat. This is why they recommended diets rich in carbohydrates pretending that they did not make people gain weight. Professor Walter WILLETT denounced this fact when he said, « by advising people to eliminate fats from their diets and recommending that they eat carbohydrates, nutritionists have contributed to spreading obesity.” Uniformed or recalcitrant nutritionists’ failure to advise their patients on which carbs to eat left people suffering from obesity to their own devices and to their tendency to eat high-GI carbs. This made their bodies secrete more insulin and generate greater amounts of surplus glucose which their bodies did not need and which was eventually stored as fat.